Humans ; Hyperparathyroidism, Secondary ; Parathyroidectomy ; Renal Insufficiency

BACKGROUND:Vocuolar-type ATPase (V-ATPase) is highly expressed in osteoclasts and especial y plays an important role in osteoclastic bone resorption. Tumor necrosis factor-αis a potent stimulator of bone resorption. However, the effect of tumor necrosis factor-αon expression and activity of V-ATPase is stil not clear.
OBJECTIVE:To investigate the mechanism of tumor necrosis factor-αto promote osteoclastic bone resorption by observing expression and activity of V-ATPase.
METHODOsteoclasts cultured in vitro were intervened by different concentrations of tumor necrosis factor-α(5, 10, 30μg/L) in order to observe the changes in expression and enzyme activity of V-ATPase and its effects on bone resorption of osteoclasts. Under an inverted microscope, we observed the formation of resorption lacunas, and bone resorption area was analyzed using Image J software.
RESULTS AND CONCLUSION:The expression and activity of V-ATPase increased significantly after 48 hours of tumor necrosis factor-αintervention and the increase of tumor necrosis factor-αconcentration might enhance this effect. In addition, osteoclastic bone resorption was promoted after intervention with tumor necrosis factor-α. The bone-resorbing capabilities of osteoclasts increased in paral el with the concentration of tumor necrosis factor-α.The results suggested that tumor necrosis factor-α, as a significant inflammatory mediator involved in the pathological process of bone resorption, not only promotes formation of osteoclasts but also enhances bone-resorbing capabilities of osteoclasts by increasing V-ATPase expression and activity.

Objective To analyze the clinical features of renal involvement associated with Behcet's disease (BD) through 1 case and to make a review of the literature in order to early diagnose and cure in time,thus decrease misdiagnosis and mistreatment.Methods This is a retrospective study.The case was diagnosed with BD and the renal damage was confirmed by renal biopsy.The clinical features and histology features were analyzed.Results The presentation of renal disease was edema,proteinuria and microscopic hematuria.The clinical spectrum of renal BD showed a wide variation.Amyloidosis (AA type),GN (nephritis),and microscopic vascular disease were the main causes of renal BD.Patients with vascular involvement had a high risk of amyloidosis and amyloidosis was the most common cause of renal failure in BD.Conclusion Kidney is one of the organs that can alter the prognosis of the BD,so the screening for renal damage must be done for each patient with this disease.Routine urine analysis and measurement of serum creatinine level are needed for early diagnosis of renal BD.Immunosuppressive drugs can be useful in selected cases.

ObjectiveTo evaluate the effects of 1,25(OH)zD3 on podocyte apoptosis in kidney of puremyein aminonueleoside nephropathy (PAN) rats. Methods Seventy-two male Sprague-Dawley rats were randomly divided into three groups: PAN model group(PAN), 1,25 (OH)2D3 treated group (T, 0.2 μg·kg-1d-1 by garages) and normal control group (NC). PAN rat model was constructed by a single intravenous injection of 100 mg/kg body weight. Renal function and 24hour urinary protein were measured at day 3, 7, 14, 21 after PAN injection. The renal tissue morphology was observed by light and electron microscope. Podocyte apeptosis was evaluated by TUNEL. Protein expressions of nephrin, TGF-β1 and p-Smad2/3 were examined by immunofluoreacence, immunohistochemistry and Western blot, respectively. Results(1)The levels of serum creafinine, BUN and 24-h urinary protein [(20.26±4.87) mg vs (1.01±0.41) mg at day 7, P ＜0.01] were significantly higher and the number of glomerular pedocyte was significantly lower [(10.9±4.2)/glomerular volume vs (31.9±6.2)/glomerular volume at day 14, P＜0.01] in PAN group compared with NC group. T group rats had less urinary protein excretion [(9.95±3.82) mg/24 h, P＜0.01] and more glomerular podocytes compared with PAN group. (2) Distribution of nephrin expression was changed from linear to granular pattern in PAN rats on day 7, nephrin mRNA and protein expressions were markedly decreased(P＜0.01), while the number of apoptotic podocyte was increased in PAN group(P＜0.01). However, higher nephrin expression and less apoptotic podocytes were found in T group (P＜0.01). (3) Compared with NC group, the mRNA and protein expression of TGF-β1 and p-Smad2/3 were higher in PAN group (P＜0.01), while 1,25 (OH)2D3 treatment abrogated PAN-induced changes in the expression of TGF-β1 and p-Smad2/3 (P＜0.01). Conclusions 1,25 (OH)2D3 can significantly suppress PAN-induced podocyte apoptosis and ameliorate proteinnuria. The beneficial effect of 1,25(OH)2D3 on podocyte may contribute to direct suppression of TGF-β signaling.

AIM: To explore the role of TGF-?_1 and signaling transduction molecule, Smad4, in the development of glomerulosclerosis. METHODS: Expression levels of TGF-?_1, Smad4, collagen Ⅰ proteins were evaluated by immunohistochemistry in renal biopsies from 38 cases with a spectrum of glomerulonephritis, and compared with 20 normal kidney tissue with image analysis system. After stimulation with TGF-?_1, expressions of endogenous Smad4 and collagen Ⅰ mRNA and proteins and its modulation by TGF?_1 were evaluated by RT-PCR and Western blotting analyses in cultured human mesangial cells. RESULTS: All types of proliferative and sclerotized glomerulonephritis showed an increased expression of TGF-?_1, Smad4 and collagen Ⅰ ompared with the 20 normal kidney tissue in glomerular (P

Objective To explore the risk factors of hypertension in patients with IgA nephropathy in South China. Methods The clinical and renal pathological data of 280 primary IgA nephropathy patients diagnosed by biopsy were analyzed to extinguish the risk factors of hypertension. Results A total of 96 patients were suffered with hypertension (34.3%). A single-variable analysis showed that the age (≥40 years), body weight (≥60 kg), absence of macrohematuria, duration of disease (≥60 months), blood urea nitrogen≥8 mmol/L, serum creatinine (≥133 μmol/L), hyperuricaemia, degree of 24 h-proteinuria (≥1.5 g), segmental glomerular lesions (≥25% ), globe glomerular sclerosis (≥10%), tubular atrophy (≥25%), interstitial fibrosis (≥25%), interstitial inflammation (≥25% ) and arteriole hypertrophy (≥10% ) were all risk factors related to hypertension; multivariate logistic regression analysis showed that serum creatinine, age, arteriole hypertrophy, body weight and 24 h-proteinuria were the independent risk factors. Conclusion Many factors were related the hypertension in patients with IgA nephropathy, while serum creatinine, age, arteriole hypertrophy, body weight and 24 h-proteinuria were the independent risk factors of hypertension.

OBJECTIVTo investigate the potential value of urine hepatitis B virus (HBV) DNA as a new noninvasive diagnostic indicator for HBV-associated glomerulonephritis (HBV-GN).

METHODSA total of 152 patients including 66 with HBV-GN, 66 with non-HBV-GN, and 20 with chronic hepatitis B (CHB) without renal disease were examined for serum and urine HBV DNA levels using polymerase chain reaction (PCR) and for 5 serum HBV markers using enzyme-linked immunosorbent assays.

RESULTSTwenty-two patients (33%) in the HBV-GN group, but none in the other two groups, were found positive for urine HBV DNA. In the diagnosis of HBV-GN, urine HBV DNA had a high specificity (0.98), a good positive predictive value (PPV, 0.96), and a modest negative predictive value (NPV, 0.60). Urine HBV DNA, alone or in combination with serum HBeAg, was superior in the diagnosis of HBV-GN to the combination of urine HBV DNA with serum HBV DNA, hepatitis B surface antigen and the hepatitis B e antigen.

CONCLUSIONUrine HBV DNA may be one of the new noninvasive diagnostic criterion for HBV-GN.

Biomarkers ; blood ; urine ; DNA, Viral ; blood ; urine ; Enzyme-Linked Immunosorbent Assay ; Glomerulonephritis ; diagnosis ; virology ; Hepatitis B Surface Antigens ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; complications ; Humans ; Polymerase Chain Reaction ; Predictive Value of Tests ; Sensitivity and Specificity

A case of anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) with ocular masses as the main manifestation was reported. The patient was a middle-aged female, the initial symptom was eye swelling, pulmonary nodules were found before eye surgery, and further examination revealed proteinuria, hematuria and renal insufficiency. Renal pathology showed ANCA-associated glomerulonephritis. The final diagnosis was eye, kidney and lung lesions caused by AAV. Treatment with glucocorticoids and cyclophosphamide resulted in improvement in eye, kidney, and pulmonary lesions. Atypical clinical manifestations of AAV may lead to delayed diagnosis, and attention should be paid to the exclusion of AAV for ocular masses of unknown cause.

OBJECTIVETo observe the effect of 11R-VIVIT on lipopolysaccharide (LPS)-induced expression of urokinase-type plasminogen activator receptor (uPAR) in podocytes.

METHODSA LPS-induced proteinuria mouse model and in vitro cultured podocytes treated with LPS were both divided into control group, LPS group and LPS+11 R-VIVIT group. The mRNA and protein expressions of uPAR in mouse kidney tissues and the podocytes were measured by real-time qPCR, laser scanning confocal microscopy and Western blotting.

RESULTSCompared with LPS group, LPS+11 R-VIVIT group showed a significantly lowered urine albumin/creatinine ratio (P<0.001) and markedly reduced mRNA and protein expressions of uPAR (PuPAR mRNA<0.001; PuPAR=0.001).

CONCLUSION11R-VIVIT can ameliorate proteinuria probably by decreasing the expression of uPAR in podocytes.

Animals ; Disease Models, Animal ; Lipopolysaccharides ; adverse effects ; Male ; Mice ; Mice, Inbred C57BL ; Oligopeptides ; pharmacology ; Podocytes ; drug effects ; metabolism ; Proteinuria ; drug therapy ; metabolism ; Receptors, Urokinase Plasminogen Activator ; metabolism

OBJECTIVETo investigate the role of IL-17 in the overproduction of autoantibodies and IL-6 overexpression by peripheral blood mononuclear cells (PBMC) of lupus nephritis (LN) patients.

METHODSFifteen consecutively hospitalized LN patients were selected as subjects and 15 healthy adults as normal controls. PBMC were obtained by Ficoll density gradient centrifugation. IgG, anti-dsDNA antibody and IL-6 protein levels were assessed using enzyme-linked immunosorbent assays (ELISA) on the supernatant of cultured PBMC of LN patients or normal controls. IL-6 mRNA levels in PBMC were measured using reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSIn medium culture, IgG, anti-dsDNA and IL-6 protein levels of the supernatant of PBMC from LN patients were significantly higher than those from normal controls (1492.1 +/- 73.2 ng/ml vs 636.7 +/- 51.9 ng/ml for IgG, 306.6 +/- 53.7 IU/ml vs 95.8 +/- 11.6 IU/ml for anti-dsDNA and 50.92 +/- 15.92 ng/ml vs 1.77 +/- 0.73 ng/ml for IL-6, all P < 0.001). In LN patients, IgG, anti-dsDNA and IL-6 protein levels were higher in the supernatants of PBMC in the IL-17-stimulated culture than the medium culture, but in normal controls, only the IL-6 protein levels were significantly higher. The increase in IgG, anti-dsDNA and IL-6 protein levels induced by IL-17 was dose-dependent and could be completely blocked by IL-17 monoclonal antibody mIgG(28) and partially blocked by dexamethasone. Similarly, IL-6 mRNA overexpression of PBMC in LN patients or normal controls induced by IL-17 was both dose- and time-dependent. During medium culture, IL-6 mRNA levels in LN patients were significantly higher than those in normal controls (1.80 +/- 0.11 vs 0.36 +/- 0.07). During stimulation with IL-17, IL-6 mRNA levels in LN patients were higher than those in normal controls (3.21 +/- 0.24 vs 1.30 +/- 0.14, P < 0.05) and also significantly higher when comparing the stimulated culture with the medium culture either in LN patients or normal control.

CONCLUSIONSIL-17 may play an important role in the pathogenesis of LN through the induction of IgG, anti-dsDNA overproduction and IL-6 overexpression of PBMC in LN patients.

Adolescent ; Adult ; Antibodies, Antinuclear ; biosynthesis ; Autoantibodies ; biosynthesis ; Female ; Humans ; Immunoglobulin G ; biosynthesis ; Interleukin-17 ; pharmacology ; Interleukin-6 ; biosynthesis ; genetics ; Leukocytes, Mononuclear ; metabolism ; Lupus Nephritis ; immunology ; Male ; RNA, Messenger ; analysis